Physical mapping studies, using restriction enzymes, nucleic acid hybridization and electron microscopy, have probed the genomes of human adenoviruses in considerable detail, revealing a complex distribution of early and late viral gene clusters. These methods have been applied to investigate DNA structure, genome expression and biological properties of incomplete adenovirus particles. Available data suggest the origin of these particles is related to events in virion assembly. This will be further tested, with emphasis on a recently developed method for in vitro association of viral DNA with empty Ad7 capsids. Results may lead to a practical method to deliver investigator-specified DNA sequences to the nuclei of susceptible cells. The potential applications of such a system for the study of recombinant DNA activity in eukaryote cells are apparent. The most abundant incomplete adenovirus particles contain DNA representing only the left 10-15 percent of the viral genome. The particles do not interfere with adenovirus infection, nor do they appear to replicate. They can transform hamster cells in culture. This positive result will be pursued in studies of malignant transformation of permissive human cells and nonpermissive cells in culture. The incomplete adenovirus particles are a potentially powerful probe for study of transcription of the single, left and early gene cluster apart from the influence of the rest of the viral genome. Transient and perhaps persistent expression of the genes associated with the incomplete particles will be studied by use of physical mapping methods with RNA and DNA from abortively infected human cells. Focus on this region of the viral genome will eventually extend to the level of DNA sequence. Further development of physical mapping technique will continue. Experments with intercalating dyes preventing branch migration in two-step hybridizations are still in progress. This approach will also be pursued beyond its original mapping rationale to develop methods of site directed in vitro mutagenesis of viral DNA.